Results 171 to 180 of about 2,026,261 (344)
Gao et al. report that circular DNA molecules created as by‐products of V(D)J recombination during lymphocyte maturation (ESCs) can replicate and be retained for much longer than previously thought in healthy cells. In BCP‐ALL cells, increased ESC abundance correlates with a greater chance of relapse likely mediated by their ability to induce genome ...
Davide Pradella, Andrea Ventura
wiley +1 more source
O09: Phenome-wide studies of hereditary transthyretin amyloidosis in the All of Us research program
Cassia Williams-Rogers +12 more
doaj +1 more source
The distribution of interspersed repeats is nonuniform and conserved in the mouse and human genomes. [PDF]
Philippe Soriano +2 more
openalex +1 more source
Aggressive prostate cancer is associated with pericyte dysfunction
Tumor‐produced TGF‐β drives pericyte dysfunction in prostate cancer. This dysfunction is characterized by downregulation of some canonical pericyte markers (i.e., DES, CSPG4, and ACTA2) while maintaining the expression of others (i.e., PDGFRB, NOTCH3, and RGS5).
Anabel Martinez‐Romero +11 more
wiley +1 more source
Human endogenous retroviruslike genome with type C pol sequences and gag sequences related to human T-cell lymphotropic viruses [PDF]
Dixie L. Mager, Jamie Freeman
openalex +1 more source
ERRFI1, a neural crest (NC)‐associated gene, was upregulated in melanoma and negatively correlated with the expression of melanocytic differentiation markers and the susceptibility of melanoma cells toward BRAF inhibitors (BRAFi). Knocking down ERRFI1 significantly increased the sensitivity of melanoma cells to BRAFi.
Nina Wang +8 more
wiley +1 more source
Structural analysis of a hepatitis B virus genome integrated into chromosome 17p of a human hepatocellular carcinoma [PDF]
Yuanyuan Zhou +5 more
openalex +1 more source
Survivin and Aurora Kinase A control cell fate decisions during mitosis
Aurora A interacts with survivin during mitosis and regulates its centromeric role. Loss of Aurora A activity mislocalises survivin, the CPC and BubR1, leading to disruption of the spindle checkpoint and triggering premature mitotic exit, which we refer to as ‘mitotic slippage’.
Hana Abdelkabir +2 more
wiley +1 more source

